Charleston, SC, United States

Medical University of South Carolina

www.musc.edu
Charleston, SC, United States

The Medical University of South Carolina opened in Charleston, South Carolina in 1824 as a small private college for the training of physicians. It is one of the oldest continually operating schools of medicine in the United States and the oldest in the Deep South. The school's main building was designed by Charleston architect Albert W. Todd. The school has expanded into a state university with a medical center and six colleges for the education of health professionals, biomedical scientists and other health care personnel. It also operates as a center for research and has a public hospital. Wikipedia.


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Patent
University of Pittsburgh and Medical University of South Carolina | Date: 2016-10-13

A compound, or a pharmaceutically acceptable salt thereof, having a structure of


Bradshaw A.D.,Medical University of South Carolina
International Journal of Biochemistry and Cell Biology | Year: 2012

The SPARC family of proteins represents a diverse group of proteins that modulate cell interaction with the extracellular milieu. The eight members of the SPARC protein family are modular in nature. Each shares a follistatin-like domain and an extracellular calcium binding E-F hand motif. In addition, each family member is secreted into the extracellular space. Some of the shared activities of this family include, regulation of extracellular matrix assembly and deposition, counter-adhesion, effects on extracellular protease activity, and modulation of growth factor/cytokine signaling pathways. Recently, several SPARC family members have been implicated in human disease pathogenesis. This review discusses recent advances in the understanding of the functional roles of the SPARC family of proteins in development and disease. © 2012 Elsevier Ltd. All rights reserved.


Walle T.,Medical University of South Carolina
Annals of the New York Academy of Sciences | Year: 2011

This paper reviews our current understanding of the absorption, bioavailability, and metabolism of resveratrol, with an emphasis on humans. The oral absorption of resveratrol in humans is about 75% and is thought to occur mainly by transepithelial diffusion. Extensive metabolism in the intestine and liver results in an oral bioavailability considerably less than 1%. Dose escalation and repeated dose administration of resveratrol does not appear to alter this significantly. Metabolic studies, both in plasma and in urine, have revealed major metabolites to be glucuronides and sulfates of resveratrol. However, reduced dihydroresveratrol conjugates, in addition to highly polar unknown products, may account for as much as 50% of an oral resveratrol dose. Although major sites of metabolism include the intestine and liver (as expected), colonic bacterial metabolism may be more important than previously thought. Deconjugation enzymes such as β-glucuronidase and sulfatase, as well as specific tissue accumulation of resveratrol, may enhance resveratrol efficacy at target sites. Resveratrol analogs, such as methylated derivatives with improved bioavailability, may be important in future research. © 2011 New York Academy of Sciences.


The question of whether cigarette smoking was associated with lung cancer was central to the expansion of epidemiology into the study of chronic diseases in the 1950s. The culmination of this era was the 1964 report of the Advisory Committee to the Surgeon General, a landmark document that included an objective synthesis of the evidence of the health consequences of smoking according to causal criteria. The report concluded that cigarette smoking was a cause of lung cancer in men and sufficient in scope that "remedial action" was warranted at the societal level. The 2014 Surgeon General's report commemorates the 50th anniversary of the 1964 report. The evidence on the health consequences of smoking has been updated many times in Surgeon General's reports since 1964. These have summarized our increasingly greater understanding of the broad spectrum of the deleterious health effects of exposure to tobacco smoke across most major organ systems. In turn, this evidence has been translated into tobacco control strategies implemented to protect the public's health. The Surgeon General report process is an enduring example of evidence-based public health in practice. Substantial progress has been made, but cigarette smoking remains one of the most pressing global health issues of our time. © The Author 2013.


Gooz M.,Medical University of South Carolina
Critical Reviews in Biochemistry and Molecular Biology | Year: 2010

This review focuses on the role of ADAM-17 in disease. Since its debut as the tumor necrosis factor converting enzyme (TACE), ADAM-17 has been reported to be an indispensible regulator of almost every cellular event from proliferation to migration. The central role of ADAM-17 in cell regulation is rooted in its diverse array of substrates: cytokines, growth factors, and their receptors as well as adhesion molecules are activated or inactivated by their cleavage with ADAM-17. It is therefore not surprising that ADAM-17 is implicated in numerous human diseases including cancer, heart disease, diabetes, rheumatoid arthritis, kidney fibrosis, Alzheimer's disease, and is a promising target for future treatments. The specific role of ADAM-17 in the pathophysiology of these diseases is very complex and depends on the cellular context. To exploit the therapeutic potential of ADAM-17, it is important to understand how its activity is regulated and how specific organs and cells can be targeted to inactivate or activate the enzyme. © 2010 Informa UK Ltd.


Silvestri G.A.,Medical University of South Carolina
Annals of Internal Medicine | Year: 2011

After the publication of the NLST (National Lung Screening Trial) results, physicians will be faced with whether to begin ordering low-dose computed tomography (LDCT) of the chest to screen for lung cancer in patients with a history of tobacco use. Despite the encouraging reduction in deaths observed by using LDCT in the NLST study population, recommending adoption of lung cancer screening in general practice is premature. © 2011 American College of Physicians.


Britten C.D.,Medical University of South Carolina
Cancer Chemotherapy and Pharmacology | Year: 2013

The PI3K/AKT/mTOR and RAS/RAF/MEK/ERK pathways are two of the most frequently dysregulated kinase cascades in human cancer. Molecular alterations in these pathways are implicated in tumorigenesis and resistance to anticancer therapies. The PI3K/AKT/mTOR and RAS/RAF/MEK/ERK pathways are known to interact with each other at several nodes, and mounting evidence suggests that dual blockade of both pathways may be required to achieve anticancer effects in certain contexts. This may include tumor types with a high frequency of RAS/RAF/MEK/ERK pathway activation, or situations in which dual pathway strategies may be required to overcome resistance to current targeted therapies. Several clinical studies are currently evaluating the combination of PI3K and MEK inhibitors in a variety of different cancers with certain types of molecular alterations. This review will summarize existing knowledge of the PI3K/AKT/mTOR and RAS/RAF/MEK/ERK pathways, the cross-talk between them, and the current generation of PI3K and MEK inhibitors that target them. The preclinical rationale for dual pathway inhibition will be discussed within the context of the major tumor types currently being explored in ongoing clinical trials, namely malignant melanoma with BRAF or NRAS mutations, and colorectal, ovarian, pancreatic, and basal-like breast cancers. The emerging clinical profile of PI3K and MEK inhibitor combinations, as reported in Phase I trials, will also be discussed. © 2013 Springer-Verlag Berlin Heidelberg.


Henggeler S.W.,Medical University of South Carolina
Annual Review of Clinical Psychology | Year: 2011

The 35-year progression of multisystemic therapy (MST) from modest university-based efficacy studies to large-scale transport to community practice settings is described in this review. The success of early efficacy research led to effectiveness trials, and their success in decreasing rates of youth rearrest and incarceration led to multisite transportability trials and adaptations of the MST model for treating youth presenting other types of challenging clinical problems. To support the transport of MST programs to community settings, an intensive quality improvement system modeled after that used in clinical trials has been implemented in community-based MST programs for the past 15 years. With the association between therapist treatment fidelity and youth outcomes well established, transportability research has demonstrated the significant roles played by clinical supervisors, expert consultants, and provider organizations in supporting therapist adherence and youth outcomes. This body of work has been facilitated by federal and state initiatives to support evidence-based services. Copyright © 2011 by Annual Reviews. All rights reserved.


Liu B.,Medical University of South Carolina
Nature communications | Year: 2010

Cytosolic HSP90 requires multiple cochaperones in folding client proteins. However, the function of gp96 (HSP90b1, grp94), an HSP90 paralogue in the endoplasmic reticulum (ER), is believed to be independent of cochaperones. Here, we demonstrate that gp96 chaperones multiple Toll-like receptors (TLRs), but not TLR3, in a manner that is dependent on another ER luminal protein, CNPY3. gp96 directly interacts with CNPY3, and the complex dissociates in the presence of adenosine triphosphate (ATP). Genetic disruption of gp96-CNPY3 interaction completely abolishes their TLR chaperone function. Moreover, we demonstrate that TLR9 forms a multimolecular complex with gp96 and CNPY3, and the binding of TLR9 to either molecule requires the presence of the other. We suggest that CNPY3 interacts with the ATP-sensitive conformation of gp96 to promote substrate loading. Our study has thus established CNPY3 as a TLR-specific cochaperone for gp96.


Grant
Agency: NSF | Branch: Cooperative Agreement | Program: | Phase: RESEARCH INFRASTRUCTURE IMPROV | Award Amount: 2.00M | Year: 2015

Non-technical description
This Research Infrastructure Improvement Track-2 Focused EPSCoR* Collaboration (RII Track-2 FEC) project involves the Medical University of South Carolina as the lead and the University of Alabama at Birmingham, Furman University, and University of South Carolina, Beaufort Campus as collaborative partners. Much of our knowledge of brain function comes from experiments using functional magnetic resonance imaging (fMRI), which directly measures blood flow to regions of the brain, but remains an indirect measure of neural activity. The precise relationship between neural events and hemodynamic response (increased blood flow) is unclear. This project will test the hypothesis that universal rules relate these two brain activities, using direct measurements in the brain and retina of mice and macaques.

Technical Description
The research will develop new instrumentation for in vivo imaging and cell subtype-specific stimulation in both the brain and the retina necessary for interpreting functional Magnetic Resonance Imaging (fMRI) measurements. These activities will help determine the extent of neurovascular coupling and provide a description of the micro-circuitry, which represents a critical and necessary step in understanding the full complexity of the brain. The consortium will track neural and vascular activity with micron-scale resolution, using two-photon microscopy and adaptive optics to measure the presence of synthetic dyes interacting with genetically encoded sensors. Cell subtype-specific stimulation will be monitored using optogenetic techniques. A computational team will analyze the data obtained to tease out hemodynamic signals. Experiments will be performed on macaques, selected because of the similarity in size and functional repertoire with the human brain. Studies in mice, where genetic and molecular tools are more readily available, will also be performed.

*Experimental Program to Stimulate Competitive Research

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